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A rare case of infectious colitis

Article  in  Gastroenterology Report · May 2015

DOI: 10.1093/gastro/gov016

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Shashank Garg Suraj Tandon

Arkansas Gastroenterology Eastern Virginia Medical School
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 Gastroenterology Report Advance Access published May 25, 2015

Gastroenterology Report, 2015, 1–3

doi: 10.1093/gastro/gov016
Case report

CASE REPORT

A rare case of infectious colitis

Aditya Kalakonda1,*, Shashank Garg2, Suraj Tandon2, Rakesh Vinayak2 and
Sudhir Dutta2
1
State University of New York (SUNY) Upstate Medical University, Syracuse, NY, USA and 2Department of
Gastroenterology, Sinai Hospital of Baltimore, Baltimore, MD, USA

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*Corresponding author. Department of Gastroenterology, Sinai Hospital of Baltimore, University of Maryland School of Medicine, 2411 W. Belvedere Ave,
Suite 305, Baltimore, MD 21215, USA. Tel: þ1-410-601-5392; Fax: þ1-410-601-5757; Email: kalakona@upstate.edu

Abstract
Methicillin-resistant Staphylococcus aureus (MRSA) is responsible for numerous infectious processes. Gastrointestinal tract
involvement is rather rare and only a handful of cases of MRSA colitis have been reported in North America. We present a
case of MRSA colitis in an adult without apparent risk factors. Abdominal computed tomography (CT) showed thickening
of the sigmoid colon, indicative of colitis, and empiric therapy with ciprofloxacin and metronidazole was started. Initial
work-up for infection—including blood and stool cultures, and stool Clostridium difficile toxin assay—was negative. The
patient’s clinical status improved but his diarrhea did not abate. Repetition of stool culture demonstrated luxuriant growth
of MRSA sensitive to vancomycin. Oral vancomycin was administered and the patient’s symptoms promptly ceased.

Key words: methicillin-resistant Staphylococcus aureus; infectious colitis; stool culture

Introduction
Enterocolitis secondary to methicillin-sensitive Staphylococcus
aureus (MSSA) has been described since the 1950s and has typi-
cally been associated with peri-operative antibiotic therapy and
gastrointestinal surgery [1]. In recent years its prevalence has
been re-assessed given the isolation of other pathogens, mainly
Clostridium difficile (C. difficile) [2]. Although MSSA has been fre-
quently isolated, methicillin-resistant Staphylococcus aureus
(MRSA) has, in rare cases, been identified as the cause of colitis.
MRSA colitis has seldom been reported in North America, with
only a very small number of documented cases. We present a
rare case of MRSA colitis in an adult without significant risk fac-
tors or history of gastroenterological illness.
Case presentation
A 34-year-old Caucasian male was brought to the emergency
room following multiple episodes of non-bilious vomiting and
non-bloody diarrhea over the previous three days. This was
associated with abdominal bloating, listlessness, decreased oral
intake and decreased urine output. The patient’s history was ob-
tained from his mother as the patient was unable to speak. She did
not notice any fever, chills, or sweating. She did not report any re-
cent hospitalization or sick contacts for the patient. His past medi-
cal history was significant for developmental delay, club foot,
neural deafness and type II diabetes. Family history was unre-
markable in terms of any infectious or gastrointestinal illnesses.
His mother was his primary carer. The patient did not have a his-
tory of alcohol, tobacco or illicit drug use. He was not taking any
medications at home and did not have any reported allergies.
Vital signs in the emergency room were significant for a tem-
perature of 38.7 C, heart rate of 153 bpm, blood pressure of 74/
43 mmHg, respiratory rate of 55 with 90% oxygen saturation on 2
L of supplemental oxygen via nasal cannula. General examina-
tion was remarkable for lethargy, dry mucous membranes, col-
lapsed neck veins, and decreased skin turgor. Abdominal
examination revealed a distended abdomen with marked left

Submitted: 19 March 2015; Revised: 19 March 2015; Accepted: 30 March 2015

C The Author(s) 2015. Published by Oxford University Press and the Digestive Science Publishing Co. Limited.
V
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/),
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1
 2 | Aditya Kalakonda et al.

lower quadrant tenderness. No guarding or rebound tenderness Discussion

was noted. Bowel sounds were remarkably decreased.
Staphylococcus aureus is a normal inhabitant of the gastrointes-
Laboratory analysis showed a white blood cell count of 20.9
tinal tract and can be cultured in many individuals as part of
cells/mL with 10% band neutrophils and 62% mature neutro-
normal bowel flora. In the mid-twentieth century, pseudomem-
phils, blood urea nitrogen 57 mg/dL, creatinine 2.75 mg/dL, bicar-
branous enterocolitis, secondary to MSSA, increased in preva-
bonate 13 mmol/L with an anion gap of 26 and lactic acid level of
lence among patients who received either peri-operative
10.3 mmol/L. Liver enzymes, total bilirubin and coagulation fac-
antibiotic therapy or who underwent major gastrointestinal sur-
tors were within normal limits. Work-up for sources of infection
gery [1–3]. MSSA was implicated as the causative agent based
included blood cultures, stool culture, stool C. difficile toxin
on positive stool cultures and enterotoxin studies; however,
polymerase chain reaction (PCR) and urine analysis.
these diagnoses were made prior to isolation of the C. difficile en-
The patient was started on intravenous fluid therapy for de-
terotoxin. Since its isolation in 1978 among patients identified
hydration, along with ciprofloxacin and metronidazole for sus-
with pseudomembranous enterocolitis, the diagnosis rate of
pected infectious colitis. Abdominal plain films showed a
MSSA enterocolitis had sharply decreased [3, 4].
distended colon, suggestive of distal colonic obstruction vs. in-
Since its discovery in 1961 MRSA, like MSSA, has become an
testinal ileus. Computed tomography (CT) scan of the abdomen
increasingly common pathogen in the nosocomial and commu-
showed thickening of the sigmoid colon with distension of the
nity environment. In the United States it is estimated that on
transverse and descending colon, consistent with colitis. The
average 94 000 patients annually are infected with MRSA, result-
patient underwent a colonoscopy, which showed severe inflam-
ing in 19 000 deaths [5]. The primary disease process associated
mation with mucosal friability and grey-white exudates extend-
with community-acquired invasive MRSA has been reported to
ing from the sigmoid to the descending colon (Figure 1). A
be bacteremia (75.2%), pneumonia (13.3%), cellulitis (9.7%), oste-

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sudden transition to fairly normal-looking colon was noted in
omyelitis (7.5%), endocarditis (6.3%), and septic shock (4.3%) [5].
the transverse colon. Multiple biopsies were taken from the af-
The nares are considered to be the primary carriage source for
fected and seemingly normal areas.
MRSA; however, the intestine and rectum have been estimated
The patient’s hypotension and lactic acidosis resolved with
to have colonization rates as high as 10% [6] and 60% [4], respec-
intravenous fluids and creatinine trended down to normal by
tively. Although MRSA is prevalent in the community, it rarely
hospital day 5, but his diarrhea did not abate. Stool culture was
poses a risk to healthy individuals. Unlike MSSA, MRSA has not
negative for Salmonella, Shigella, Campylobacter, and Yersinia.
been frequently isolated as a cause of colitis.
Blood cultures, urine analysis and stool C. difficile toxin assay
MRSA colitis has been documented in a small subset of indi-
were also negative. Colonoscopic biopsies showed mild active
viduals in Asian literature [7]. No similar extent of cases within
colitis with fibrino-purulent exudates. Given the negative work-
similar patient populations has been reported in western litera-
up for infectious colitis and active inflammation of pathology,
ture. To the best of our knowledge, we present the sixth case of
the patient was started on intravenous corticosteroids and
MRSA colitis in the western literature (Table 1) [8–12]. In pub-
mesalamine rectal enemas for proctitis from suspected ulcera-
lished data, there seems to be some relationship between recent
tive colitis. Additionally, a repeat stool specimen was sent for
antibiotic use, acid-suppressive therapy and recent abdominal
culture. On the sixth day following admission, the repeat stool
surgery, and the development of MRSA colitis [13, 14].
culture came back positive for heavy growth of MRSA. The pa-
Specifically, MRSA colitis has been found to occur most com-
tient was subsequently started on vancomycin 125 mg orally
monly in patients who have undergone recent gastric surgery.
QID for 14 days. After the institution of vancomycin, the pa-
Generally these patients developed MRSA colitis two to seven
tient’s symptoms promptly resolved. He was taken off the corti-
days after surgery. It has been postulated that the initiation of
costeroids. His repeat stool culture 30 days later was negative
broad-spectrum antibiotics, elevation of gastric pH juices due to
for MRSA, indicating cure.
anti-peptic ulcer drugs, and lack of peristalsis all contribute to the
development of MRSA-related colitis in these patients [6]. As wit-
nessed in our patient, MRSA can cause spontaneous, invasive,
gastrointestinal disease despite the absence of any risk factors.
MRSA colitis is characterized by high fever, abdominal dis-
tension and watery diarrhea that often leads to severe dehydra-
tion, shock, a sharp increase in white cell counts and
sometimes multi-organ failure. In patients with hospital-ac-
quired diarrhea of unknown etiology, risk factors such as hemi-
gastrectomy and broad spectrum antibiotic use should alert the
physician to considering the possibility of staphylococcal en-
terocolitis [9, 13, 14]. The reported literature suggests that stool
gram stain and culture is the mainstay of the diagnosis.
Imaging studies and colonoscopy can help in ruling out other
disorders or confirming the diagnosis. Oral vancomycin has
been the mainstay of therapy for MSSA enterocolitis and using
a similar regimen for 10–14 days in MRSA colitis also seems to
be an effective treatment modality (Table 1). Although vanco-
mycin-resistant Staphylococcus aureus has been increasing in
prevalence [15], there have been no reported cases of resistance
to vancomycin in MRSA colitis.
It should also be mentioned that it is equally likely that our
patient may have developed MRSA colitis as a result of initiation
Figure 1. Endoscopic findings
 Infectious colitis | 3

Table 1. Review of reported cases of MRSA colitis in the western literature

Case Age Sex Presentation Risk factors Laboratory Radiographic / Diagnostic Treatment
evaluation endoscopic findings method

Taylor et al. 71 M Diarrhea, pruritis, re-

Crohn’s disease, history of WBC: 11.2x109/L; Not available Stool culture Oral vancomycin x 8
[8], 1993 duced urine output previous right Cr: 747 mol/L days. No follow-up
hemicolectomy stool culture
Schiller 64 F Nausea, vomiting, wa- Remote splenectomy and Not available Sigmoidoscopy: patchy Stool culture Oral vancomycin: un-
et al. [9], tery diarrhea x 1 hemigastrectomy, sigmoid colitis known duration. No
1998. week Klebsiella pneumonia follow-up stool
treated with multiple an- culture
tibiotics 1 week prior to
symptom onset
McPherson 43 F Watery diarrhea, col- Hysterectomy and prophy- WBC: 18 000/mm3; X-ray of abdomen: di- Stool culture Oral vancomycin x 10
et al. [10], icky abdominal lactic antibiotics 1 day CRP: 102 mg/L lated loops of days. No follow-up
2005 pain, vomiting x 1 prior to symptom onset, bowel; stool culture
day healthcare worker Sigmoidoscopy:
normal
Cheng et al. 39 M High output ileos- Appendectomy and prophy- WBC: 14 800/mm3; Not available Stool culture IV vancomycin: un-
[11], 2006 tomy, x 1 day lactic antibiotics 9 days CRP: 99 mg/L known duration.
and Hartmann’s proce- Follow-up stool cul-
dure 5 days prior to ture showed MRSA
symptom onset colonization
Clarke et al. 60 F Diarrhea, fever, bright Health care worker CRP: 14 times upper CT of abdomen: pan Stool culture Oral vancomycin: un-

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[12], 2012 red blood per rec- limit of normal colitis; known duration. No
tum, x 4 weeks Colonoscopy: pan follow-up stool
colitis with ulcera- culture
tions in transverse
colon
Current 34 M Diarrhea, vomiting, None identified WBC: 20 900/mm3; X-ray of abdomen: co- Stool culture Oral vancomycin x 14
case abdominal disten- BUN:57 mg/dL; lonic distension; CT days. Follow-up stool
sion x 3 days Cr: 27.5 mg/L; of abdomen: left- culture negative for
CO2: 13 mmol/L; sided colitis; MRSA
Lactic acid: Colonoscopy: pseu-
10.3 mmol/L domembranous
colitis

BUN ¼ blood urea nitrogen; Cr ¼ creatinine; CRP ¼ C-reactive protein; F ¼ Female; M ¼ Male; MRSA ¼ methicillin-resistant Staphylococcus aureus; WBC ¼ white blood count

of empiric broad-spectrum antibiotic therapy. This could have
resulted in an imbalance in normal colonic flora, leading to an
excess growth of MRSA. Given its complications, physicians
should be aware of its rapid clinical course and initiate prompt
treatment with vancomycin to prevent decline in a patient’s
clinical course. Unrecognized and untreated MRSA colitis may
pose a significant strain on the patient’s hospital course, while
incurring additional hospital costs.
Conflict of interest statement: none declared.
References
1. Thakkar S and Agrawal R. A Case of Staphylococcus aureus Entero-
colitis: A Rare Entity. Gastroenterol Hepatol (N Y) 2010;6:115–17.
2. Kotler DP and Sordillo EM. A Case of Staphylococcus aureus Enter-
ocolitis: A Rare Entity. Gastroenterol Hepatol (N Y) 2010;6:117–19.
3. Froberg MK, Palavecino E, Dykoski R et al. Staphylococcus au-
reus and Clostridium difficile cause distinct pseudomembra-
nous intestinal diseases. Clin Infect Dis 2004;39:747–50.
4. Tan MJ. Staphylococcus aureus enterocolitis: an underrecog-
nized mimic of Clostridium difficile. Infect Dis Clin Pract (Baltim
Md) 2008;16:207–8.
5. Klevens RM, Morrison MA, Nadle J et al. Invasive methicillin-
resistant Staphylococcus aureus infections in the United
States. JAMA 2007;298:1763–71.
6. Takeuchi K, Tsuzuki Y, Ando T et al. Clinical studies of enteri-
tis caused by methicillin resistant Staphylococcus aureus.
Eur J Surg 2001;167:293–6.
7. Iwata K, Doi A, Fukuchi T et al. A systematic review for pursu-
ing the presence of antibiotic associated enterocolitis caused
by methicillin resistant Staphylococcus aureus. BMC Infect Dis
2014;14:247.
8. Taylor M, Ajayi F, Almond M. Enterocolitis caused by methi-
cillin-resistant Staphylococcus aureus. Lancet 1993;342:804.
9. Schiller B, Chiorazzi N, Farber BF. Methicillin-resistant
Staphylococcal enterocolitis. Am J Med 1998;105:164–6
10. McPherson S, Ellis R, Fawzi H et al. Postoperative methicillin-
resistant Staphylococcus aureus enteritis following hysterec-
tomy: a case report and review of the literature. Eur J
Gastroenterol Hepatol 2005;17:1225–7.
11. Cheng A, Wade A, Harris O et al. Postoperative enteritis due to
methicillin-resistant Staphylococcus aureus. ANZ J Surg 2006;
76:763.
12. Clarke K and Baidoo L. Methicillin–resistant Staphylococcal
aureus (MRSA) colitis: is there a problem? Int J Colorectal Dis
2012;27:417–18.
13. Watanabe H, Sato S, Kurita S et al. [Clinical study of 18 pa-
tients whom MRSA was detected from stool: especially about
comparison enterocolitis with colonization]. Kansenshogaku
Zasshi 1996;70:1170–5.
14. Sekikawa T. [The study of cases with infection by methicillin-
resistant Staphylococcus aureus]. Rinsho Byori 1990;38:
1211–18.
15. Tenover FC, Biddle JW, Lancaster MV. Increasing resistance to
vancomycin and other glycopeptides in Staphylococcus au-
reus. Emerg Infect Dis 2001;7:327–32.

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